hypercalcaemia_malignancy

most common metabolic emergency in Oncology
symptoms if rapid rise or very high levels > 3.0 mmol/l
cardiac, neural, muscular neurophysiology altered
Mechanism:
- bony involvement: M. myeloma, Breast, Lung
- parathormone like substance: Squamous cell lung
- osteoclast activating factor: Lymphoma
40 % of patients with Multiple myeloma/ Breast

little correlation between Ca ++ levels and presence/severity of symptoms
Acute increase :
- marked CNS: personality ⇒ coma
Chronic increase :
- General: itch
- Neuro: fatigue, weakness, apathy, perception + behaviour change, stupor, coma
- Renal: polyuria, polydipsia
- GIT: anorexia, nausea, vomiting, constipation, pain

ionized calcium is responsible for neuromuscular dysfunction
- ⇒ interpret with Se. albumin, pH + phosporus
- IONIZED Ca++ = measured Ca++ + (40 – serum albumin g/l) x 0.02
  - > 3.0 corrected ⇒ consider inpatient treatment
ECG: short QT interval
U + E:
- to ensure adequacy of response to fluids and diuretics
- exclude concomitant hypokalaemia

aims:
- 1) Rehydration
- 2) increase Ca++ excretion
- 3) decrease Ca++ removal from bone
- 4) decrease Ca++ intake
- 5) Rx underlying malignancy
consider CVP + PAP monitoring +/- IDC
rehydrate:
- IV fluids (1⇒ 2 L NS rapidly, aim 3-6 l/day):
  - Rate depends on fluid status/CVP, UO, cardiac Fx
- most malignancy induced Ca++ responds (stimulates renal tubular Ca++ secretion)
once rehydrated:
- IV frusemide 80mg
  - ⇒ renal Ca++ excretion (req. N renal FX- 100ml/hr)
replace K+/Mg++ may fall rapidly with rehdration/diuretics
bisphosphonates (on ward) ⇒ bind to hydroxyapatite, inhibits osteoclast activity
haemodialysis/peritoneal dialysis against a low/no calcium dialysate
treatment of underlying malignancy (except breast, cease radiotherapy until calcium level normalises )
corticosteroids for long term control